Approximately 45 million acres of grassland are occupied by tall fescue in the continental United States alone. These grasslands are primarily used to support beef cow herds for the production and sale of cull beef, feeder and stocker calves and herd replacements. Most of the tall fescue grasslands are severely infested with an endophyte fungus, Acremonium coenophialum, which is responsible for a syndrome commonly known as tall fescue toxicosis.
Endophyte infected tall fescue plants produce and contain pyrrolizidine alkaloids. Pyrrolizidine alkaloids cause three main toxic effects in domestic farm animals such as horses, cattle and sheep. The alkaloids exert their effects on tissue by causing necrosis, by inhibiting mitosis and thereby causing megalocytosis and/or by acting directly on blood vessels and causing edema and vascular disease. Typical symptoms include, for example, hepatic lesions of the liver and intestitial pneumonia in the lungs (Effects of Poisonous Plants on Livestock, by Richard F. Keeler, Kent R. Van Kampen & Lynn F. James, Academic Press, 1978).
Tall fescue toxicosis severely limits the productivity of as many as twelve million cattle in terms of conception, milk production and live weight gain. Approximately ten million feeder calves and stocker cattle also suffer from tall fescue toxicosis each year. Consequently, cattle from tall fescue areas, principally Kentucky, Tennessee, Missouri, Virginia and southern Ohio, Indiana and Illinois, are discounted by stocker and finishing operations.
All together, tall fescue toxicosis in cattle and sheep cause losses in animal productivity estimated in the hundreds of millions of U.S. dollars annually. A need, therefore exists, for a method of effectively treating tall fescue toxicosis in domestic farm animals.
During our studies of the tall fescue toxicosis problem, we have determined that the pyrrolizidine alkaloids of the endophyte infected tall fescue grasses are chemically similar to and may function as cosubstrates for the thiaminase mediated destruction of thiamin. As such, we hypothesize that tall fescue toxicosis may be a form of thiamin deficiency.
In testing this hypothesis, we have discovered that cattle suffering from tall fescue toxicosis may effectively be treated with feed supplemented with thiamin.
Thiamin is a naturally occuring substance involved as a cofactor in many enzyme systems of plant and animal cells. Thiamin is chemically synthesized in large amounts and widely used as a nutritional supplement for monogastric animals such as man, and chickens. Thiamin has also been advocated as a means of alleviating stress such as shipping fever and has been studied extensively in feedlot systems. Thiamin is, however, not generally used in ruminant nutrition for it is generally considered as unnecessary. This is because ruminants such as cattle include organisms capable of synthesizing sufficient amounts of thiamin for use by the animal within their rumen.
Thiamin has also been proposed as a method of treating polioencephalomalacia or PEM. We, however, believe we are the first to propose and demonstrate that thiamin may be used to effectively treat tall fescue toxicosis.